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Table 3 EBV-associated miRNAs and their roles in Burkitt lymphoma: Diagnostic, prognostic, and therapeutic implications

From: From virus to cancer: Epstein–Barr virus miRNA connection in Burkitt's lymphoma

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References

Specific miRNAs

miR-378a-3p is upregulated in BL and its inhibition reduces BL cell growth by targeting genes like MNT and IRAK4 involved in growth regulation

[31]

miRNA Expression Profiles

miR-BART6-3P and miR-BART17-5P are frequently observed in BL and can be used as diagnostic or prognostic markers and potential therapeutic targets

[43]

Chromosomal Aberrations

1q gains in BL are associated with dysregulation of miRNAs such as hsa-miR-181a and hsa-miR-181b which are upregulated in EBV-negative BL

[32]

CXCL-11 Targeting

EBV miRNA BHRF1-3 targets the IFN-inducible T-cell attracting chemokine CXCL-11/I-TAC potentially serving as an immunomodulatory mechanism in BL

[95]

miR-197 and IL-6R

EBV-BART6-3p and cellular miR-197 synergistically reduce the expression of IL-6R compromising the immune defense in EBV-positive BL

[19]

Differential Expression

Significant differences in the expression of viral miRNAs and target genes like LIN28B, CGNL1, and GCET2 between EBV-positive and EBV-negative BL

[96]

miR-10a-5p

Downregulation of hsa-miR-10a-5p in jaw tumors and nonsurvivors of endemic BL suggesting its role in tumor resilience and patient outcomes

[40]

miR-150

Re-expression of miR-150 in EBV-positive BL induces differentiation and reduces proliferation by targeting c-Myb

[65]

miRNA as Biomarkers

Specific miRNAs such as miR-155 and miR-21 are overexpressed in BL and can serve as biomarkers for diagnosis and prognosis. These miRNAs are involved in various cellular pathways that promote cancer growth

[97]

HIV-1 Influence

HIV-1 exposure downregulates hsa-miR-200c-3p enhancing BL cell migration and promoting oncogenesis. This interaction highlights the complexity of BL in HIV-positive patients

[98]

Epigenetic Regulation

EBV miRNAs can influence the epigenetic landscape of BL cells affecting gene expression and contributing to cancer development. This includes changes in DNA methylation and histone modification

[99]

Therapeutic Perspectives

Strategies to convert latency I tumors (like BL) to latency II/III are being investigated to sensitize tumors to T-cell mediated killing

[100]

Therapeutic Resistance

Dysregulation of miRNAs in BL can lead to resistance to conventional therapies. For example, miR-34a downregulation is associated with resistance to chemotherapy

[101]

Hit-and-Run Hypothesis

EBV-microRNAs detection is proposed as a more specific and sensitive tool to recognize EBV vestiges in BL even in cases diagnosed as EBV-negative by conventional methods

[102]

Immune Evasion

EBV miRNAs increase viremia and virus-associated lymphomas by dampening antigen recognition by adaptive immune responses

[103]

  1. BL: Burkitt lymphoma, EBV: Epstein–Barr virus, miRNA: microRNA, IFN: Interferon, IL-6R: Interleukin-6 receptor, 1q: Long arm of chromosome 1, CXCL-11/I-TAC: C-X-C motif chemokine ligand 11/Interferon-inducible T-cell alpha chemoattractant, MNT: Max Network Transcriptional Repressor, IRAK4: Interleukin-1 Receptor-Associated Kinase 4, LIN28B: Lin-28 Homolog B, CGNL1: Cingulin-Like 1, GCET2: Germinal Center-Associated Nuclear Protein 2, hsa-miR: Homo sapiens MicroRNA, c-Myb: Avian Myeloblastosis Viral Oncogene Homolog